Autism is a developmental disorder that affects brain function, interfering with reasoning ability, imagination, communication, and social interaction. Formerly a rare disorder, autism has increased in the last decade by 300% to 500% in the United States and many other countries. Clearly, a means of prevention and treatment of what is now an epidemic are needed. A variety of different types of autism treatments premised on a variety of different theories regarding the development of autism (e.g., that it is due to a persistent atypical viral infection in patients administered live attenuated combination vaccinations, that it results from toxic metals such as mercury in the context of autoimmunity, that it results from affecting retinoid receptors in the brain through disruption of the G-alpha protein, and other theories) presently exist. However, what is needed is an approach to autism that addresses the underlying causes of autism, as opposed to one that merely treats or even masks the symptoms.
An approach that treats the symptoms and potentially the causes of autism is the individualized nutrient therapy for autism, such as reported in Isaacson et al., Journal of Applied Nutrition, 48, 110-118 (1996), the Autism Research Publication “Patient Ratings of Behavioral Effects of Drugs, Nutrients, and Diets”, ARI Publ. 34, Autism Research Institute, 4182 Adams Avenue, San Diego, Calif. 92116, September 2000, as well as in other references. This individualized therapy relies on treatment optimized for the individual's particular chemical imbalance, with particular nutrients emphasized in certain imbalances, and others avoided.
Recently, methods of testing for a predisposition to autism, for preventing or delaying the onset of autism once a predisposition for autism has been detected, and for treating the symptoms of autism once autism has developed, have been described based on the surprising discovery of an inborn error of metal metabolism underlying the etiology of autism, which is signaled, among other things, by substantially elevated Cu/Zn levels in blood. (See, Walsh et al., “Disordered Metal Metabolism in a Large Autism Population”, Abstract NR823, American Psychiatric Association Annual Meeting, New Orleans, La., May 10, 2001, and “Metallothionein and Autism”, October 2001, publication of the Pfeiffer Treatment Center, Naperville, Ill. (each incorporated by reference in their entireties)). This suggests that effective autism prevention and/or treatment can be achieved by (1) early infant screening for disordered metal metabolism followed by treatment of any disorder uncovered, and (2) vigilant avoidance of toxic metals for at-risk children (e.g., children identified as having a predisposition for the development of autism).
Furthermore, these findings suggest that a disorder of the function of metallothioneins (MTs) underlies autism. Metallothioneins are short, linear, cysteine-rich proteins composed of between sixty-one and sixty-eight amino acids. They have been highly conserved over time and throughout a wide array of species, suggesting that they are essential for life. All human MTs contain twenty cysteine residues and have an “s” configuration with extraordinary metal-binding capability. MTs bind with zinc, lead, copper, mercury, silver, and cadmium both in the intestinal tract and in the liver. In terms of the relativity affinity of metals for metallothionein, mercury exhibits the highest affinity for MTs, and copper, cadmium, lead, and zinc exhibit successively lower affinities for MTs. Functions of MTs include (1) limitation of the amounts of Hg, Pb, and other toxic metals which can be absorbed by the body, and (2) sequestering of toxic metals in “safe” MT molecules of fairly high stability.
The consequences of insufficient metallothionein activity (i.e., also described herein as “MT dysfunction”) include, but are not limited to, the following:
(1) reduced ability to prevent absorption of Cu, Hg, Pb, and Cd into the portal bloodstream;
(2) dramatically increased toxicity of Hg, Pb, and Cd and other heavy metals in cells and membranes;
(3) impaired homeostasis of Cu and Zn resulting in Cu overload and Zn depletion in brain and periphery;
(4) impaired neuronal development which could result in incomplete maturation of the gastrointestinal tract and brain;
(5) impaired immune function;
(6) dopamine depletion and norepinephrine overload; and
(7) occupation of enzyme sulfhydryl groups by Hg and other heavy metals.
However, in particular, metallothionein inactivity (and accordingly, MT dysfunction) greatly increases sensitivity to toxic heavy metals.
Accordingly, the present invention provides novel and non-obvious nutrient supplements that, among other things, are effective for promoting metallothioneins in a person. The invention also provides an effective generic treatment for autism involving administration of the nutrient supplements, which preferably can be employed to treat autism once diagnosed, or to prevent or delay the onset of autism in persons predisposed to the development of autism. Moreover, the invention provides generic treatment involving administration of nutrient supplements that optionally can be employed in the treatment of other diseases, disorders, or conditions that would benefit from promotion of metallothioneins. These and other objects and advantages of the present invention, as well as additional inventive features, will be apparent from the following description of the invention provided herein.